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Table 4 Comparative analysis of pseudocyesis, PCOS and major depressive disorder traits according to the variables included in Table 2 a

From: Endocrinology and physiology of pseudocyesis

Variables included in Table 2 Pseudocyesis PCOS Major depressive disorder
Amenorrhea Yes Yes [36, 59] No [60]
Galactorrhea Yes Yes b No [60]
LH/FSH ratio Increased Increased c ?
Frequency of LH pulses Increased Increased c Decreased frequency and dysrhythmic pulses [60]
T levels Elevated Elevated[61] Elevated [62]
E2 levels Within the (broad) normal ranges Within the (broad) normal ranges[63] Decreased levels in the follicular phased
P levels Within or slightly higher than the follicular phase range Within either the follicular phase range or the lutheal phase range e Normal P levels on the first day after menstruation [62] and higher P levels in the luteal phase [64]
GH levels Decreased nocturnal peaks and normal diurnal episodic secretion Low, normal or elevated levels with impaired diurnal secretion [65] Decreased nocturnal secretion [66]
PRL levels Normal (putative occult hyperprolactinemia), slightly elevated or distinctly elevated Hyperprolactilemia (10-15% of PCOS women) [36] Normal [62]
DHEAS levels Minimally elevated Elevated (20-33% of PCOS women [67]) Normal [68]
Cortisol levels Normal Normal [67] Disturbed diurnal rhythms, higher evening levels and accentuated post-awakening surge [69]
Response of ACTH to dexamethasone Escape from suppression ? Some individuals escape from suppression [42]
Response of cortisol to dexamethasone Suppression Suppression [70] Some individuals escape from suppression [42]f
Response of LH and FSH to GnRH Normal increase Higher increase in LH and normal increase in FSH [71] Normal increase[62]
Response of GH to TRH Paradoxical increase Paradoxical increase (≈42% of PCOS women [46]) Paradoxical increase [43]
Response of TSH to TRH Normal or small increase ? Small increase [43, 44]
Response of GH to dopamine agonists Deficient or reduced increase Deficient or reduced increase [72, 73]g Normal [74]or reduced increase[75–77]
Response of LH and/or PRL to opioid receptor antagonists No increase in LH and PRL Small increase in LH and no increase in PRL [78, 79] Increase in LH [80]h
  1. aCommon traits of pseudocyesis, PCOS and/or major depressive disorder are highlighted using bold text.
  2. bAlthough the true incidence of galactorrhea in PCOS remains unclear and is probably only 1 or 2%, a study published in 1980 [81] reported that ≈ 24% of PCOS women show galactorrhea irrespectively of the concomitant presence of either hyperprolactinemia (≈14%) or normoprolactinemia (≈10%).
  3. cPCOS women have increased GnRH pulse frequency because of androgen-mediated decreased GnRH sensitivity to P feedback inhibition. The higher GnRH pulse frequency increases LH pulsatility and favors LH production over FSH (for reviews, see McCartney et al. [36] and Burt-Solorzano et al. [59]).
  4. dWhereas untreated premenopausal women suffering from major depression display E2 levels on the first day after menstruation similar to those found in healthy age-matched control women [62], they often have plasma levels of E2 in the follicular phase significantly lower than control healthy women (for reviews, see Swaab et al. [82] and Williams et al. [60]), although they exhibit higher amplitudes of diurnal E2 rhythms [83].
  5. eLevels in PCOS women show the typical changes associated with either anovulation (P deficiency, i.e., within the follicular phase range) or ovulation (within the luteal phase range) [84, 85]. Note that nearly 12% of oligo- or amenorrheic PCOS women show signs of spontaneous ovulation based on random P assessment [86].
  6. fSome of the discrepancies between cortisol and ACTH responses to dexamethasone in major depressed individuals may be due to the low sensitivity and specificity of the ACTH assays used in some studies [42].
  7. gThe hyperandrogenemia in PCOS may contribute to the relatively reduced response of GH to dopamine agonists (for review, see Spiliotis [49]).
  8. hThe study by Martín del Campo et al. [80] is methodologically flawed. In particular, they analyzed a heterogeneous group of women with major depression (4 post-menopausic, 2 eumenorrheic and one with irregular cycles) and did not control for the phase of the menstrual cycle. In addition, they used both women and men as control subjects. Despite these methodological deficiencies, there is evidence of dysregulated endogenous opioid emotion regulation circuitry in women with major depressive disorder [87].
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